Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414, USA.
J Immunol. 2012 Oct 1;189(7):3293-7. doi: 10.4049/jimmunol.1201439. Epub 2012 Aug 31.
Several recent studies reported that Krüppel-like factor (KLF)2 controls trafficking, development, and function of B cells. Conditional B cell KLF2 knockout mice have increased numbers of marginal zone B cells and decreased numbers of B1 phenoytpe cells. However, it was unclear whether KLF2 is required for B1 B cell development, survival, or phenotypic maintenance. We show that B1 phenotype B cells are present in neonatal mice with B cell-specific KLF2 deficiency, suggesting that B1 differentiation can occur even in the absence of KLF2. Furthermore, by use of an inducible knockout strategy, we show that deletion of KLF2 in mature B1 cells causes loss of phenotypic markers associated with B1 cell identity, but it has a minimal effect on short-term cell survival. Taken together, our findings suggest that KLF2 is necessary for the maintenance of B1 cell identity rather than differentiation or survival of the population.
几项最近的研究报告称,Krüppel 样因子(KLF)2 控制 B 细胞的运输、发育和功能。条件性 B 细胞 KLF2 敲除小鼠的边缘区 B 细胞数量增加,B1 表型细胞数量减少。然而,尚不清楚 KLF2 是否是 B1 B 细胞发育、存活或表型维持所必需的。我们发现,在 B 细胞特异性 KLF2 缺陷的新生小鼠中存在 B1 表型 B 细胞,这表明即使没有 KLF2,B1 分化也可以发生。此外,通过使用诱导型敲除策略,我们表明在成熟的 B1 细胞中删除 KLF2 会导致与 B1 细胞身份相关的表型标记丢失,但对短期细胞存活的影响很小。综上所述,我们的研究结果表明,KLF2 对于 B1 细胞身份的维持是必需的,而不是该群体的分化或存活所必需的。